Described herein are systems, methods and devices for improving cardiac function. The systems, methods, and devices described herein may relate generally to treating heart disease, particularly heart failure, and more specifically, to systems, methods, and devices for delivering a partitioning device to a patient's ventricle.
Heart failure annually leads to millions of hospital visits internationally. Heart failure is the description given to a myriad of symptoms that can be the result of the heart's inability to meet the body's demand for blood flow. In certain pathological conditions, the ventricles of the heart become ineffective in pumping the blood, causing a back-up of pressure in the vascular system behind the ventricle.
The reduced effectiveness of the heart is usually due to an enlargement of the heart. A myocardial ischemia may, for example, cause a portion of a myocardium of the heart to lose its ability to contract. Prolonged ischemia can lead to infarction of a portion of the myocardium (heart muscle) wherein the heart muscle dies and becomes scar tissue. Once this tissue dies, it no longer functions as a muscle and cannot contribute to the pumping action of the heart. When the heart tissue is no longer pumping effectively, that portion of the myocardium is said to be hypokinetic, meaning that it is less contractile than the uncompromised myocardial tissue. As this situation worsens, the local area of compromised myocardium may in fact bulge out as the heart contracts, further decreasing the heart's ability to move blood forward. When local wall motion moves in this way, it is said to be dyskinetic, or akinetic. The dyskinetic portion of the myocardium may stretch and eventually form an aneurysmic bulge. Certain diseases may cause a global dilated myopathy, i.e., a general enlargement of the heart when this situation continues for an extended period of time.
As the heart begins to fail, diastolic pressures increase, which stretches the ventricular chamber prior to contraction and greatly increases the pressure in the heart. In response, the heart tissue reforms to accommodate the chronically increased filling pressures, further increasing the work that the now compromised myocardium must perform.
A further example is congestive heart failure (CHF), characterized by a progressive enlargement of the heart, particularly the left ventricle. CHF is a major cause of death and disability in the United States and elsewhere. As a patient's heart enlarges, it pumps less efficiently and, in time, the heart becomes so enlarged that it cannot adequately supply blood to the body. The fraction of blood within the left ventricle that is pumped forward at each stroke, commonly referred to as the “ejection fraction”, is typically about sixty percent for a healthy heart. A congestive heart failure patient typically has an ejection fraction of 40% or less, and as a consequence, is chronically fatigued, physically disabled, and burdened with pain and discomfort. Further, as the heart enlarges, heart valves lose the ability to close adequately. An incompetent mitral valve allows regurgitation of blood from the left ventricle back into the left atrium, further reducing the heart's ability to pump blood.
Congestive heart failure can result from a variety of conditions, including viral infections, incompetent heart valves, ischemic conditions in the heart wall, or a combination of these conditions. Prolonged ischemia and occlusion of coronary arteries can result in myocardial tissue in the ventricular wall dying and becoming scar tissue. Once a portion of myocardial tissue dies, that portion no longer contributes to the pumping action of the heart. As the disease progresses, a local area of compromised myocardium can bulge during the heart contractions, further decreasing the heart's ability to pump blood, and further reducing the ejection fraction.
In the early stages of heart failure, drug therapy is presently the most commonly prescribed treatment. Drug therapy typically treats the symptoms of the disease and may slow the progression of the disease, but it does not cure the disease. Presently, the only treatment considered curative for heart failure is heart transplantation, but these procedures are high risk, invasive, and costly. Further, there is a shortage of hearts available for transplant, many patients fail to meet transplant-recipient qualifying criteria.
Much effort has been directed toward the development of surgical and device-based treatments for heart failure. Surgical procedures have been developed to dissect and remove weakened portions of the ventricular wall in order to reduce heart volume. As is the case with heart transplant, these procedures are invasive, risky, and costly, and many patients do not qualify medically for the procedure. Other efforts to treat heart failure include the use of an elastic support placed around the heart to prevent further deleterious remodeling, and mechanical assist devices and completely mechanical hearts have been developed. Recently, improvements have been made in treating patients with heart failure by implanting pacing leads in both sides of the heart in order to coordinate the contraction of both ventricles of the heart. While these various procedures and devices have been found to be successful in providing some relief from heart failure symptoms and in slowing disease progression, none has been able to stop the course of the disease.
However, ventricular partitioning devices offer a solution for treating heart failure. These devices generally function to partition a patient's ventricle into a productive region and a non-productive region. For such devices to function properly, they are positioned in a specific location within the patient's heart chamber. Delivery of a partitioning device may be made complicated by the anatomy of a patient and by aspects or characteristics of the delivery device or partitioning device itself. Thus, it would be beneficial to provide devices, systems and methods for delivering and deploying a partitioning device in a patient's ventricle.